Nearly 70 years ago, the association between reduction in renal mass and subsequent glomerular injury was established. Later the pathologic changes were attributed to adaptive hemodynamic changes in the residual nephrons. This relationship seems to exist in a number of experimental animal species, as well as humans. Among the various hemodynamic changes that occur within residual nephrons, the increase in glomerular pressure is the most important in generating subsequent pathologic changes. The renin-angiotensin-aldosterone system seems to contribute to the intrarenal pressure. Both angiotensin and aldosterone participate. Increases in glomerular pressure appear to act on the mesangial compartment causing it to increase its cell number and matrix volume. Deleterious interactions between higher pressures, increased capillary volume, and a relatively fixed podocyte number also appear to contribute to the sclerotic process. Endothelial cell changes occur perhaps in response to direct hemodynamic stimuli, but their role in the sclerotic process is less clear than those of mesangial and glomerular epithelial cells.
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